ArticleThe EMBO journal2001
Binding of Ikaros to the lambda5 promoter silences transcription through a mechanism that does not require heterochromatin formation.
Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 148 citations in OpenAlex.
- Article
- IKAROS: from chromatin organization to transcriptional elongation control.Cell death and differentiation · 2025Review
- AIOLOS-Associated Inborn Errors of Immunity.Journal of clinical immunology · 2024Review
- A Point Mutation in IKAROS ZF1 Causes a B Cell Deficiency in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Research Note: Circular RNA expressing in different developmental stages of the chicken bursa of Fabricius.Poultry science · 2020Article
- Review
- Hierarchical assembly and disassembly of a transcriptionally active RAG locus in CD4The Journal of experimental medicine · 2019Article
- Dual Roles for Ikaros in Regulation of Macrophage Chromatin State and Inflammatory Gene Expression.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Article
- Genetic Mutations and Epigenetic Modifications: Driving Cancer and Informing Precision Medicine.BioMed research international · 2017Review
- Direct interaction of Ikaros and Foxp1 modulates expression of the G protein-coupled receptor G2A in B-lymphocytes and acute lymphoblastic leukemia.Oncotarget · 2016Article
- Biochemical and cellular characterization of transcription factors binding to the hyperconserved core promoter-associated M4 motif.BMC genomics · 2016Article
- Regulation of gene expression dynamics during developmental transitions by the Ikaros transcription factor.Genes & development · 2015Article
- Characterization and dynamics of pericentromere-associated domains in mice.Genome research · 2015Article
- Gene repositioning within the cell nucleus is not random and is determined by its genomic neighborhood.Epigenetics & chromatin · 2015Article
- Ikaros is absolutely required for pre-B cell differentiation by attenuating IL-7 signals.The Journal of experimental medicine · 2013Article
- Direct protein interactions are responsible for Ikaros-GATA and Ikaros-Cdk9 cooperativeness in hematopoietic cells.Molecular and cellular biology · 2013Article
- Function of Ikaros as a tumor suppressor in B cell acute lymphoblastic leukemia.American journal of blood research · 2013Article
- Heterochromatin and gene positioning: inside, outside, any side?Chromosoma · 2012Article
- Congenital pancytopenia and absence of B lymphocytes in a neonate with a mutation in the Ikaros gene.Pediatric blood & cancer · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ikaros family of proteins are DNA binding factors required for correct development of B and T lymphocytes. Cytogenetic studies have shown that these proteins form complexes with pericentromeric heterochromatin in B cells, and the colocalization of transcriptionally silent genes with these complexes suggests that Ikaros could silence transcription by recruiting genes to heterochromatin. Here we show that a site in the lambda5 promoter that binds Ikaros and Aiolos is required for silencing of lambda5 expression in activated mature B cells. Analysis of methylation and nuclease accessibility indicates that the silenced lambda5 gene is not heterochromatinized in B cells, despite being associated with pericentromeric heterochromatin clusters. We also found that a promoter mutation, which affects Ikaros-mediated silencing of lambda5 expression, is not rescued in a transgenic line that has the gene integrated into pericentromeric heterochromatin. Our results indicate that the Ikaros proteins initiate silencing of lambda5 expression through a direct effect on the promoter with localization to pericentromeric heterochromatin likely to affect the action of Ikaros on regulatory sequences rather than causing heterochromatinization of the gene.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.